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      Effects of alpha lipoic acid and its R+ enantiomer supplemented to hyperbaric oxygen therapy on interleukin-6, TNF-αand EGF production in chronic leg wound healing

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          Abstract

          Lipoic acid (LA) and hyperbaric oxygenation therapy (HBOT) improve chronic wound healing.

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          Pathophysiology of acute wound healing.

          Jie Li, Juan Chen, Robert Kirsner (2007)
          Wound healing is a complex process that can be divided into at least 3 continuous and overlapping processes: an inflammatory reaction, a proliferative process leading to tissue restoration, and, eventually, tissue remodeling. Wound healing processes are strictly regulated by multiple growth factors and cytokines released at the wound site. Although the desirable final result of coordinated healing would be the formation of tissue with a similar structure and comparable functions as with intact skin, regeneration is uncommon (with notable exceptions such as early fetal healing); healing however results in a structurally and functionally satisfactory but not identical outcome. Alterations that disrupt controlled healing processes would extend tissue damage and repair. The pathobiologic states may lead to chronic or nonhealing wounds or excessive fibrosis.
          Article 0 comments Cited 342 times – based on 0 reviews     Review now
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            Hyperbaric oxygen: its mechanisms and efficacy.

            Stephen R Thom (2010)
            This article outlines therapeutic mechanisms of hyperbaric oxygen therapy and reviews data on its efficacy for clinical problems seen by plastic and reconstructive surgeons. The information in this review was obtained from the peer-reviewed medical literature. Principal mechanisms of hyperbaric oxygen are based on intracellular generation of reactive species of oxygen and nitrogen. Reactive species are recognized to play a central role in cell signal transduction cascades, and the discussion will focus on these pathways. Systematic reviews and randomized clinical trials support clinical use of hyperbaric oxygen for refractory diabetic wound-healing and radiation injuries; treatment of compromised flaps and grafts and ischemia-reperfusion disorders is supported by animal studies and a small number of clinical trials, but further studies are warranted. Clinical and mechanistic data support use of hyperbaric oxygen for a variety of disorders. Further work is needed to clarify clinical utility for some disorders and to hone patient selection criteria to improve cost efficacy.
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              Vascular permeability factor, an endothelial cell mitogen related to PDGF.

              Victor T. Warren, G Krivi, K Sanzo … (1989)
              Vascular permeability factor (VPF) is a 40-kilodalton disulfide-linked dimeric glycoprotein that is active in increasing blood vessel permeability, endothelial cell growth, and angiogenesis. These properties suggest that the expression of VPF by tumor cells could contribute to the increased neovascularization and vessel permeability that are associated with tumor vasculature. The cDNA sequence of VPF from human U937 cells was shown to code for a 189-amino acid polypeptide that is similar in structure to the B chain of platelet-derived growth factor (PDGF-B) and other PDGF-B-related proteins. The overall identity with PDGF-B is 18%. However, all eight of the cysteines in PDGF-B were found to be conserved in human VPF, an indication that the folding of the two proteins is probably similar. Clusters of basic amino acids in the COOH-terminal halves of human VPF and PDGF-B are also prevalent. Thus, VPF appears to be related to the PDGF/v-sis family of proteins.
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                Author and article information

                Journal
                Title: Journal of Enzyme Inhibition and Medicinal Chemistry
                Abbreviated Title: Journal of Enzyme Inhibition and Medicinal Chemistry
                Publisher: Informa UK Limited
                ISSN (Print): 1475-6366
                ISSN (Electronic): 1475-6374
                Publication date Created: January 31 2013
                Publication date (Print): January 30 2013
                Volume: 29
                Issue: 2
                Pages: 297-302
                Article
                DOI: 10.3109/14756366.2012.759951
                PubMed ID: 23360079
                SO-VID: a70b50b2-d8c9-4076-a617-4ce5703b6a33
                Copyright © © 2013
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